Upregulation of voluntary alcohol intake, behavioral sensitivity to stress, and amygdala crhr1 expression following a history of dependence
Open accessAbstract
Background A history of alcohol dependence recruits increased voluntary alcohol intake and sensitivity to stress. Corticotropin-releasing hormone (CRH) has been implicated in this transition, but underlying molecular mechanisms remain unclear.Methods A postdependent state was induced using intermittent alcohol exposure. Experiments were carried out following > or =3 weeks of recovery to eliminate contributions of acute withdrawal. Voluntary alcohol consumption was assessed in a two-bottle, free choice procedure. Behavioral sensitivity to stress was examined using fear suppression of behavior in a punished drinking (Vogel) conflict test. Effects of forced swim stress on voluntary alcohol intake were examined as a function of exposure history. Expression of Crh, Crhr1, and Crhr2 transcripts was analyzed by in situ hybridization histochemistry.Results Alcohol drinking was upregulated long-term following a history of dependence. Fear suppression of behavior was selectively potentiated in postdependent animals. This persisted 3 months after alcohol exposure and was reversed by the selective CRH-R1 antagonist 3-(4-Chloro-2-morpholin-4-yl-thiazol-5-yl)-8-(1-ethylpropyl)-2,6-dimethyl-imidazo[1,2-b]pyridazine (MTIP) (10 mg/kg). Forced swim stress increased alcohol intake in postdependent animals but not in control animals. Behavioral changes were paralleled by an upregulation of Crhr1 transcript expression within basolateral (BLA) and medial (MeA) amygdala and Crh messenger RNA (mRNA) in central amygdala (CeA). In contrast, Crhr2 expression was down in the BLA.Conclusions Neuroadaptations encompassing amygdala CRH signaling contribute to the behavioral phenotype of postdependent animals.
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“At the molecular level, increased ethanol intake following CIE or the limited access binge-drinking model drinking in the dark (DID), correlates with increased CeA CRF expression (Sommer et al., 2008, Lowery-Gionta et al., 2012).”
BackgroundAlcoholism, corticotropin-releasing factor, and molecular genetic allostasis
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- Authors
- Sommer, W. H., Rimondini, R., Hansson, A. C., Hipskind, P. A., Gehlert, D. R., Barr, C. S., & Heilig, M. A.
- Affiliations
- National Institutes of Health (US)
- University of Bologna (IT)
- Eli Lilly (United States) (US)
- Corresponding author
- Heilig, Markus A.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2008-01
- Volume
- 63
- Issue
- 2
- Pages
- 139-145
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2045358091
- Cited by
- 309
- References
- 59
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 12 · 2023: 10 · 2022: 10 · 2021: 10 · 2020: 11 · 2019: 17 · 2018: 20 · 2017: 17 · 2016: 23 · 2015: 17 · 2014: 26 · 2013: 15 · 2012: 22
- FWCI
- 8.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- alcoholism, voluntary ethanol consumption, stress sensitivity, corticotropin-releasing factor, CRH receptor 1, CRH receptor 2, amygdala, basolateral amygdala, central amygdala, medial amygdala, Vogel conflict test, forced swim stress, neural adaptation, alcohol withdrawal
- MeSH terms
- CRF Receptor, Type 1, Alcohol Drinking, Alcoholism, Amygdala, Animals, Behavior, Animal, Disease Models, Animal, Male, Pyridazines, Stress, Physiological, Thiazoles, Time Factors, Gene Expression, Rats, Wistar, In Situ Hybridization, Receptors, Corticotropin-Releasing Hormone, Rats
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